Glucocorticoid is a hormone which causes the metabolic disorder, such as hyperglycemia, insulin resistance, obesity, hyperlipidemia, hypertension and the like, and is not only produced from adrenal glands but also converted from the inactive form into the active form at the tissue level and acts via its receptor.
11β-Hydroxysteroid dehydrogenase (11β-HSD) is an enzyme which catalyzes this conversion, and the presence of two subtypes is known. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) is an enzyme which converts the inactive form into the active form and its expression is high in the liver, and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is an enzyme which converts the active form into the inactive form and its expression is high in the kidney. As the relation of 11β-HSD1 with metabolic diseases, increased activity of 11β-HSD1 in the fat tissue of obese people is known (Non-Patent Document 1), and it has been reported that the 11β-HSD1 activity shows high correlation with BMI as an index of the degree of obesity, with HOMA-IR as an index of insulin resistance, and with fasting blood glucose level (Non-Patent Document 2). In addition, it has been reported that a transgenic mouse in which 11β-HSD1 was fat tissue-selectively over-expressed shows insulin resistance, visceral fat type obesity, hyperlipidemia and hypertension, together with increase of glucocorticoid in the fat tissue (Non-Patent Documents 3 and 4) and that an 11β-HSD1 knockout mouse shows improvement of glucose tolerance, lowering of blood triglyceride and increase of HDL-cholesterol (Non-Patent Document 5).
Accordingly, it is expected that an 11β-HSD1-selective inhibitor will suppress glucocorticoid action in tissues by inhibiting conversion into the active form glucocorticoid, and, as a result, correct the metabolic disorders such as hyperglycemia, insulin resistance, obesity, hyperlipidemia, hypertension and the like caused by glucocorticoid.
In addition, since it has been reported that a non-selective 11β-HSD inhibitor carbenoxolone improves the lowering of insulin secretion in mouse pancreatic (β-cell caused by the addition of inactive glucocorticoid (Non-Patent Document 6), there is a possibility that an 11β-HSD1 inhibitor not only improves insulin resistance but also corrects hyperglycemia by accelerating insulin secretion.
11β-HSD1 is also known to be highly expressed in the brain, while 11β-HSD2 is rarely expressed in the brain (Non-Patent Document 7).
As the correlation between glucocorticoid and dementia patients, in patients suffering from Alzheimer's disease, an increase in concentration of an active form of glucocorticoid (cortisol) in the saliva or blood (Non-Patent Documents 8 and 9), HPA axis disorder (Non-Patent Document 10), correlation between cortisol concentration and brain atrophy value (Non-Patent Document 8) and the like were confirmed. In addition, language or memory disorder can be confirmed by administering cortisol or glucocorticoid drug formulations to normal persons or Alzheimer's disease patients (Non-Patent Documents 11 and 12). Also, as the correlation between 11β-HSD1 and cognition, an improvement action in language memory by administration of nonselective 11β-HSD inhibitor to type II diabetes patients (Non-Patent Document 7), and improvement action for cognition disorders in aged 11β-HSD1 knockout mice (Non-Patent Document 13) and the like were reported.
Based on these points, it is expected that the 11β-HSD1 inhibitor suppresses the action of glucocorticoid in the brain through inhibition of the conversion into an active-form glucocorticoid, and as a result, remedies cognition disorders induced by glucocorticoid.
In addition to dementia, diseases of the central nervous system, such as schizophrenia (Non-Patent Document 14), depression (Non-Patent Document 15), anxiety (Non-Patent Document 16), post-traumatic stress disorder (PTSD) (Non-Patent Document 17), attention deficit/hyperactivity disorder (AD/HD) (Non-Patent Document 18), panic disorder (Non-Patent Document 19), somnipathy (Non-Patent Document 20), which are greatly related to stress and in which an HPA axis disorder, an increase in cortisol in the blood plasma or the like is recognized, are also expected to be remedied by the 11β-HSD1 inhibitor.
As other diseases in which 11β-HSD1 is involved, osteoporosis (Non-Patent Document 21) and glaucoma (Non-Patent Document 22) are known, and improving effects of 11β-HSD1 inhibitor on these diseases are expected.
The following Patent Documents 1 to 14 are known as triazole derivatives having an inhibitory action against 11β-HSD1.
A triazole derivative represented by the formula (A) is reported in Patent Document 1. However, this triazole derivative has an indispensable structure in which an adamantyl group is bonded to a triazole ring directly or through methylene.

(In the formula, R1 indicates adamantyl which may be substituted and X indicates CH2 or a single bond. Refer to this publication for other symbols.)
A triazole derivative represented by the formula (B) is reported in Patent Document 2.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (C) is reported in Patent Documents 3 and 4.

(Refer to these publications for the symbols in the formula)
A triazole derivative represented by the formula (D) is reported in Patent Document 5.

(In the formula, X indicates O or S. Refer to this publication for other symbols.)
A condensed triazole derivative represented by the formula (E) is reported in Patent Document 6.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (F) is reported in Patent Document 7.

(Z in the formula indicates —(CH(R14))p-, —(CH(R14))p-N(R16)—(CH(R15))q- or compound represented by the following formula.

Refer to this publication for other symbols)
A compound represented by the formula (G) which include a wide range of compound is reported in Patent Document 8. However, the compound of the present invention is not specifically disclosed therein.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (H) is reported in Patent Document 9.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (J) is reported in Patent Document 10.

(In the formula, R1 represents a heterocyclic group or —N(R0)—R4, and A and B represent lower alkyl or a cycloalkyl ring together with the carbon atom to which they bond. Refer to this publication for other symbols.)
A triazole derivative represented by the formula (K) is reported in Patent Document 11.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (L) is reported in Patent Document 12.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (M) is reported in Patent Document 13.

(Refer to this publication for the symbols in the formula.)
A triazole derivative represented by the formula (N) is reported in Patent Document 14.

(In the formula, R1 represents aryl or heteroaryl. Refer to this publication for the other symbols.)